Disturbance of autophagy-lysosome signaling molecule expression in human gastric adenocarcinoma
Autophagy is classified as type II programmed cell death and may participate in tumorigenesis. However, changes in autophagy-lysosome signaling and the relationship between the apoptotic cascade and gastric cancer cells have not been fully elucidated. The present study investigated the induction of...
Gespeichert in:
| Veröffentlicht in: | Oncology letters 2014-03, Vol.7 (3), p.635-640 |
|---|---|
| Hauptverfasser: | , , , , , , |
| Format: | Artikel |
| Sprache: | eng |
| Schlagworte: | |
| Online-Zugang: | Volltext |
| Tags: |
Tag hinzufügen
Keine Tags, Fügen Sie den ersten Tag hinzu!
|
| container_end_page | 640 |
|---|---|
| container_issue | 3 |
| container_start_page | 635 |
| container_title | Oncology letters |
| container_volume | 7 |
| creator | WEI, SHAO-HUA LI, WEI LIU, YANG GAO, DE-KANG PAN, JUN GU, CHUN-WEI WU, HAO-RONG |
| description | Autophagy is classified as type II programmed cell death and may participate in tumorigenesis. However, changes in autophagy-lysosome signaling and the relationship between the apoptotic cascade and gastric cancer cells have not been fully elucidated. The present study investigated the induction of autophagy in poorly differentiated human gastric adenocarcinoma. Immunoblotting revealed markedly induced autophagy in low grade differentiated gastric adenocarcinoma, indicated by elevation of microtubule-associated protein 1 light chain 3-I/II conversion and Beclin 1 in human gastric carcinomas. In addition, the diffuse (poorly differentiated) subtype showed significantly elevated Lamp2 and cathepsin B protein levels. Concomitantly, significant induction of anti-apoptotic events were indicated by changes in B-cell lymphoma 2 (Bcl-2) and X-linked inhibitor of apoptosis protein levels. Notably, confocal laser microscope data indicated co-expression of Bcl-2 and Beclin 1 in poorly differentiated human gastric adenocarcinoma. Results of this study indicate that the autophagy-lysosome signaling participates in poorly differentiated human gastric adenocarcinoma and there are intracellular links between autophagic signaling and the apoptotic cascade. |
| doi_str_mv | 10.3892/ol.2013.1773 |
| format | Article |
| fullrecord | <record><control><sourceid>gale_pubme</sourceid><recordid>TN_cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3919863</recordid><sourceformat>XML</sourceformat><sourcesystem>PC</sourcesystem><galeid>A426827909</galeid><sourcerecordid>A426827909</sourcerecordid><originalsourceid>FETCH-LOGICAL-c633t-e839bb5f4660cbb10f5c29530961ca394ab9ad9c091a298daa77b4613ad1c9e83</originalsourceid><addsrcrecordid>eNptkktr3DAUhU1pacI0u66LoVC6qKd62HpsCiF9pBDopl2La1m2FWRpKtmh8-8rk3QmUyItJKTv3CuOTlG8xmhLhSQfg9sShOkWc06fFeeYS1JhJMjzw57XZ8VFSrcoj4ZhIdjL4ozUDeGIyfNCfbZpXmILXpsy9CUsc9iNMOwrt08hhcmUyQ4enPVDOQVn9OJMaf7soknJBl9aX47LBL4cIM3R6hI644OGqK0PE7wqXvTgkrl4WDfFr69ffl5dVzc_vn2_urypNKN0roygsm2bvmYM6bbFqG80kQ1FkmENVNbQSuikRhIDkaID4LytGabQYS2zelN8uq-7W9rJdNr4OYJTu2gniHsVwKrTG29HNYQ7RSWWIr9hU7x_KBDD78WkWU02aeMceBOWpLAgrBE1a1b07X_obVhi9ihTkhJG64azIzWAM8r6PuS-ei2qLmvCBOESyUxtn6Dy7MxkdfCmt_n8RPDukWA04OYxBbfM-TPSKfjhHtQxpBRNfzADI7WGRwWn1vCoNTwZf_PYwAP8LyrHxmkHvrNdSEd3XYV4hWiFGG3oX-Dry-4</addsrcrecordid><sourcetype>Open Access Repository</sourcetype><iscdi>true</iscdi><recordtype>article</recordtype><pqid>1932634576</pqid></control><display><type>article</type><title>Disturbance of autophagy-lysosome signaling molecule expression in human gastric adenocarcinoma</title><source>Spandidos Publications Journals</source><source>PubMed Central</source><source>EZB Electronic Journals Library</source><creator>WEI, SHAO-HUA ; LI, WEI ; LIU, YANG ; GAO, DE-KANG ; PAN, JUN ; GU, CHUN-WEI ; WU, HAO-RONG</creator><creatorcontrib>WEI, SHAO-HUA ; LI, WEI ; LIU, YANG ; GAO, DE-KANG ; PAN, JUN ; GU, CHUN-WEI ; WU, HAO-RONG</creatorcontrib><description>Autophagy is classified as type II programmed cell death and may participate in tumorigenesis. However, changes in autophagy-lysosome signaling and the relationship between the apoptotic cascade and gastric cancer cells have not been fully elucidated. The present study investigated the induction of autophagy in poorly differentiated human gastric adenocarcinoma. Immunoblotting revealed markedly induced autophagy in low grade differentiated gastric adenocarcinoma, indicated by elevation of microtubule-associated protein 1 light chain 3-I/II conversion and Beclin 1 in human gastric carcinomas. In addition, the diffuse (poorly differentiated) subtype showed significantly elevated Lamp2 and cathepsin B protein levels. Concomitantly, significant induction of anti-apoptotic events were indicated by changes in B-cell lymphoma 2 (Bcl-2) and X-linked inhibitor of apoptosis protein levels. Notably, confocal laser microscope data indicated co-expression of Bcl-2 and Beclin 1 in poorly differentiated human gastric adenocarcinoma. Results of this study indicate that the autophagy-lysosome signaling participates in poorly differentiated human gastric adenocarcinoma and there are intracellular links between autophagic signaling and the apoptotic cascade.</description><identifier>ISSN: 1792-1074</identifier><identifier>EISSN: 1792-1082</identifier><identifier>DOI: 10.3892/ol.2013.1773</identifier><identifier>PMID: 24527069</identifier><language>eng</language><publisher>Greece: D.A. Spandidos</publisher><subject>Apoptosis ; Autophagy ; Autophagy (Cytology) ; Beclin 1 ; Cancer ; Cathepsins ; Gastric cancer ; Genetic aspects ; human gastric carcinomas ; Kinases ; lysosome ; Medical prognosis ; Metastasis ; Microscopy ; Oncology ; Physiological aspects ; Polyclonal antibodies ; Proteins ; Risk factors ; Statistical analysis ; Stomach cancer ; Studies ; Tumorigenesis</subject><ispartof>Oncology letters, 2014-03, Vol.7 (3), p.635-640</ispartof><rights>Copyright © 2014, Spandidos Publications</rights><rights>COPYRIGHT 2014 Spandidos Publications</rights><rights>Copyright Spandidos Publications UK Ltd. 2014</rights><rights>Copyright © 2014, Spandidos Publications 2014</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c633t-e839bb5f4660cbb10f5c29530961ca394ab9ad9c091a298daa77b4613ad1c9e83</citedby><cites>FETCH-LOGICAL-c633t-e839bb5f4660cbb10f5c29530961ca394ab9ad9c091a298daa77b4613ad1c9e83</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3919863/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC3919863/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,723,776,780,881,5555,27903,27904,53769,53771</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/24527069$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>WEI, SHAO-HUA</creatorcontrib><creatorcontrib>LI, WEI</creatorcontrib><creatorcontrib>LIU, YANG</creatorcontrib><creatorcontrib>GAO, DE-KANG</creatorcontrib><creatorcontrib>PAN, JUN</creatorcontrib><creatorcontrib>GU, CHUN-WEI</creatorcontrib><creatorcontrib>WU, HAO-RONG</creatorcontrib><title>Disturbance of autophagy-lysosome signaling molecule expression in human gastric adenocarcinoma</title><title>Oncology letters</title><addtitle>Oncol Lett</addtitle><description>Autophagy is classified as type II programmed cell death and may participate in tumorigenesis. However, changes in autophagy-lysosome signaling and the relationship between the apoptotic cascade and gastric cancer cells have not been fully elucidated. The present study investigated the induction of autophagy in poorly differentiated human gastric adenocarcinoma. Immunoblotting revealed markedly induced autophagy in low grade differentiated gastric adenocarcinoma, indicated by elevation of microtubule-associated protein 1 light chain 3-I/II conversion and Beclin 1 in human gastric carcinomas. In addition, the diffuse (poorly differentiated) subtype showed significantly elevated Lamp2 and cathepsin B protein levels. Concomitantly, significant induction of anti-apoptotic events were indicated by changes in B-cell lymphoma 2 (Bcl-2) and X-linked inhibitor of apoptosis protein levels. Notably, confocal laser microscope data indicated co-expression of Bcl-2 and Beclin 1 in poorly differentiated human gastric adenocarcinoma. Results of this study indicate that the autophagy-lysosome signaling participates in poorly differentiated human gastric adenocarcinoma and there are intracellular links between autophagic signaling and the apoptotic cascade.</description><subject>Apoptosis</subject><subject>Autophagy</subject><subject>Autophagy (Cytology)</subject><subject>Beclin 1</subject><subject>Cancer</subject><subject>Cathepsins</subject><subject>Gastric cancer</subject><subject>Genetic aspects</subject><subject>human gastric carcinomas</subject><subject>Kinases</subject><subject>lysosome</subject><subject>Medical prognosis</subject><subject>Metastasis</subject><subject>Microscopy</subject><subject>Oncology</subject><subject>Physiological aspects</subject><subject>Polyclonal antibodies</subject><subject>Proteins</subject><subject>Risk factors</subject><subject>Statistical analysis</subject><subject>Stomach cancer</subject><subject>Studies</subject><subject>Tumorigenesis</subject><issn>1792-1074</issn><issn>1792-1082</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2014</creationdate><recordtype>article</recordtype><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNptkktr3DAUhU1pacI0u66LoVC6qKd62HpsCiF9pBDopl2La1m2FWRpKtmh8-8rk3QmUyItJKTv3CuOTlG8xmhLhSQfg9sShOkWc06fFeeYS1JhJMjzw57XZ8VFSrcoj4ZhIdjL4ozUDeGIyfNCfbZpXmILXpsy9CUsc9iNMOwrt08hhcmUyQ4enPVDOQVn9OJMaf7soknJBl9aX47LBL4cIM3R6hI644OGqK0PE7wqXvTgkrl4WDfFr69ffl5dVzc_vn2_urypNKN0roygsm2bvmYM6bbFqG80kQ1FkmENVNbQSuikRhIDkaID4LytGabQYS2zelN8uq-7W9rJdNr4OYJTu2gniHsVwKrTG29HNYQ7RSWWIr9hU7x_KBDD78WkWU02aeMceBOWpLAgrBE1a1b07X_obVhi9ihTkhJG64azIzWAM8r6PuS-ei2qLmvCBOESyUxtn6Dy7MxkdfCmt_n8RPDukWA04OYxBbfM-TPSKfjhHtQxpBRNfzADI7WGRwWn1vCoNTwZf_PYwAP8LyrHxmkHvrNdSEd3XYV4hWiFGG3oX-Dry-4</recordid><startdate>20140301</startdate><enddate>20140301</enddate><creator>WEI, SHAO-HUA</creator><creator>LI, WEI</creator><creator>LIU, YANG</creator><creator>GAO, DE-KANG</creator><creator>PAN, JUN</creator><creator>GU, CHUN-WEI</creator><creator>WU, HAO-RONG</creator><general>D.A. Spandidos</general><general>Spandidos Publications</general><general>Spandidos Publications UK Ltd</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>3V.</scope><scope>7X7</scope><scope>7XB</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>AN0</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>K9.</scope><scope>M0S</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><scope>7X8</scope><scope>5PM</scope></search><sort><creationdate>20140301</creationdate><title>Disturbance of autophagy-lysosome signaling molecule expression in human gastric adenocarcinoma</title><author>WEI, SHAO-HUA ; LI, WEI ; LIU, YANG ; GAO, DE-KANG ; PAN, JUN ; GU, CHUN-WEI ; WU, HAO-RONG</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c633t-e839bb5f4660cbb10f5c29530961ca394ab9ad9c091a298daa77b4613ad1c9e83</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2014</creationdate><topic>Apoptosis</topic><topic>Autophagy</topic><topic>Autophagy (Cytology)</topic><topic>Beclin 1</topic><topic>Cancer</topic><topic>Cathepsins</topic><topic>Gastric cancer</topic><topic>Genetic aspects</topic><topic>human gastric carcinomas</topic><topic>Kinases</topic><topic>lysosome</topic><topic>Medical prognosis</topic><topic>Metastasis</topic><topic>Microscopy</topic><topic>Oncology</topic><topic>Physiological aspects</topic><topic>Polyclonal antibodies</topic><topic>Proteins</topic><topic>Risk factors</topic><topic>Statistical analysis</topic><topic>Stomach cancer</topic><topic>Studies</topic><topic>Tumorigenesis</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>WEI, SHAO-HUA</creatorcontrib><creatorcontrib>LI, WEI</creatorcontrib><creatorcontrib>LIU, YANG</creatorcontrib><creatorcontrib>GAO, DE-KANG</creatorcontrib><creatorcontrib>PAN, JUN</creatorcontrib><creatorcontrib>GU, CHUN-WEI</creatorcontrib><creatorcontrib>WU, HAO-RONG</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Health Medical collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni)</collection><collection>ProQuest Central UK/Ireland</collection><collection>British Nursing Database</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><collection>MEDLINE - Academic</collection><collection>PubMed Central (Full Participant titles)</collection><jtitle>Oncology letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>WEI, SHAO-HUA</au><au>LI, WEI</au><au>LIU, YANG</au><au>GAO, DE-KANG</au><au>PAN, JUN</au><au>GU, CHUN-WEI</au><au>WU, HAO-RONG</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Disturbance of autophagy-lysosome signaling molecule expression in human gastric adenocarcinoma</atitle><jtitle>Oncology letters</jtitle><addtitle>Oncol Lett</addtitle><date>2014-03-01</date><risdate>2014</risdate><volume>7</volume><issue>3</issue><spage>635</spage><epage>640</epage><pages>635-640</pages><issn>1792-1074</issn><eissn>1792-1082</eissn><abstract>Autophagy is classified as type II programmed cell death and may participate in tumorigenesis. However, changes in autophagy-lysosome signaling and the relationship between the apoptotic cascade and gastric cancer cells have not been fully elucidated. The present study investigated the induction of autophagy in poorly differentiated human gastric adenocarcinoma. Immunoblotting revealed markedly induced autophagy in low grade differentiated gastric adenocarcinoma, indicated by elevation of microtubule-associated protein 1 light chain 3-I/II conversion and Beclin 1 in human gastric carcinomas. In addition, the diffuse (poorly differentiated) subtype showed significantly elevated Lamp2 and cathepsin B protein levels. Concomitantly, significant induction of anti-apoptotic events were indicated by changes in B-cell lymphoma 2 (Bcl-2) and X-linked inhibitor of apoptosis protein levels. Notably, confocal laser microscope data indicated co-expression of Bcl-2 and Beclin 1 in poorly differentiated human gastric adenocarcinoma. Results of this study indicate that the autophagy-lysosome signaling participates in poorly differentiated human gastric adenocarcinoma and there are intracellular links between autophagic signaling and the apoptotic cascade.</abstract><cop>Greece</cop><pub>D.A. Spandidos</pub><pmid>24527069</pmid><doi>10.3892/ol.2013.1773</doi><tpages>6</tpages><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 1792-1074 |
| ispartof | Oncology letters, 2014-03, Vol.7 (3), p.635-640 |
| issn | 1792-1074 1792-1082 |
| language | eng |
| recordid | cdi_pubmedcentral_primary_oai_pubmedcentral_nih_gov_3919863 |
| source | Spandidos Publications Journals; PubMed Central; EZB Electronic Journals Library |
| subjects | Apoptosis Autophagy Autophagy (Cytology) Beclin 1 Cancer Cathepsins Gastric cancer Genetic aspects human gastric carcinomas Kinases lysosome Medical prognosis Metastasis Microscopy Oncology Physiological aspects Polyclonal antibodies Proteins Risk factors Statistical analysis Stomach cancer Studies Tumorigenesis |
| title | Disturbance of autophagy-lysosome signaling molecule expression in human gastric adenocarcinoma |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-24T20%3A37%3A46IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-gale_pubme&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Disturbance%20of%20autophagy-lysosome%20signaling%20molecule%20expression%20in%20human%20gastric%20adenocarcinoma&rft.jtitle=Oncology%20letters&rft.au=WEI,%20SHAO-HUA&rft.date=2014-03-01&rft.volume=7&rft.issue=3&rft.spage=635&rft.epage=640&rft.pages=635-640&rft.issn=1792-1074&rft.eissn=1792-1082&rft_id=info:doi/10.3892/ol.2013.1773&rft_dat=%3Cgale_pubme%3EA426827909%3C/gale_pubme%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=1932634576&rft_id=info:pmid/24527069&rft_galeid=A426827909&rfr_iscdi=true |